ライフサイエンスコーパス: LTD

1 LTD induction requires CB1R in astroglial cells (but not

2 LTD thus provides a cellular mechanism for information s

3 LTD was absent in CB1 knock-out mice but preserved in he

4 LTD-like cortical plasticity is similar between AD and H

5 the catalytically-dead mutant did not affect LTD induction.

6 KII can indeed mediate not only LTP but also LTD through regulated substrate selection; however, in t

7 of visual spatial attention on LTP-like and LTD-like plasticity in the human motor cortex.

8 frequency AP-EPSP pairing, with both LTP and LTD absent under control conditions but present after SK

9 ian induction of distinct traces for LTP and LTD and their subsequent timing-dependent transformation

10 Additionally, LTP and LTD are correlated with dendritic spine enlargement and

11 s of the molecular events leading to LTP and LTD are known, experimenters often report problems in us

12 We also demonstrate that, although LTP and LTD are normal in P21 arg(-/-) slices, both forms of pla

13 However, LTP and LTD are not static, but their induction threshold is adj

14 sformation of eligibility traces for LTP and LTD as a plausible synaptic substrate for reward-based l

15 eakened output of D2-MSNs, occluding LTP and LTD at these synapses, respectively.

16 l striatum, we demonstrate that both LTP and LTD can be sequentially induced in the same D2-expressin

17 idase family of proteins) suppresses LTP and LTD in the primary visual cortex of the mouse.

18 t-LTD were significantly larger than LTP and LTD obtained by modulating the frequency and duration of

19 Because the balance of LTP and LTD plays a critical role in activity-dependent synaptic

20 wever, in Tg mice, the magnitudes of LTP and LTD stayed constant across development.

21 potentials and synaptic plasticity (LTP and LTD).

22 positive associative interaction of LTP and LTD, cross-capture, was altered in these mice.

23 These fundamental properties of LTP and LTD, Hebbian induction and NMDAR dependence, have not be

24 ent to drive NMDA receptor-dependent LTP and LTD, respectively.

25 tivation threshold that lies between LTP and LTD.

26 pendent synaptic plasticity, such as LTP and LTD.

27 of the networks responsible for both LTP and LTD.

28 on (6 month) basal synaptic transmission and LTD were also affected.

29 The alpha1-AR LTD was initiated by postsynaptic alpha1-ARs but mediate

30 We also assess the relationship between LTD and synaptic pruning in the context of recent findin

31 CA1 LTD as inhibition of JAK or STAT blocked LTD induction and prevented NMDA-induced AMPA (alpha-ami

32 ta-PrP(C)-mGlu5R interplay in mediating both LTD facilitation and LTP inhibition, encompassing NMDAR-

33 emory, can be inactivated and reactivated by LTD and LTP, respectively.

34 JAK-STAT signaling was critical for TA-CA1 LTD as inhibition of JAK or STAT blocked LTD induction a

35 TA-CA1 LTD requires NMDA receptor activation and is independent

36 Cerebellar LTD depends on the activation of calcium/calmodulin-depe

37 Mice with enhanced cerebellar LTD, due to double knockout (DKO) of MHCI H2-K(b)/H2-D(b

38 red both in acute slices or using a chemical LTD protocol in cultured neurons but did not affect hipp

39 By contrast, LTD-induced spine removal of AKAP79/150 required its dep

40 DCS-LTD is abolished with an mGluR5 negative allosteric modu

41 in vitro induces a long-term depression (DCS-LTD) of excitatory synaptic strength in both human and m

42 from brief DCS application into durable DCS-LTD.

43 However, DCS-LTD persists despite either gamma-aminobutyric acid type

44 dpoints were liver transplantation or death (LTD) and hepatopancreatobiliary malignancy, respectively

45 cal JAK-STAT signaling in activity-dependent LTD at TA-CA1 synapses and provide valuable insight into

46 A novel CB1-dependent LTD was induced in GABA cells that was dependent on meta

47 We show that dopamine-dependent LTD of NMDAR-mediated transmission profoundly disrupts n

48 In particular, exaggerated mGluR-dependent LTD is featured in fragile X syndrome, but the mechanism

49 slices rescues the enhanced mGluR-dependent LTD phenotype observed in FXS mice.

50 , also restores the level of mGluR-dependent LTD to that observed in wild-type animals.

51 rdinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo.

52 ynaptic incorporation during NMDAR-dependent LTD.

53 ynapses via the mechanism of NMDAR-dependent LTD.

54 mGlu5 receptor-dependent LTD in AS mice was sensitive to the protein synthesis in

55 Long-term potentiation (LTP) and depression (LTD) at glutamatergic synapses are intensively investiga

56 long-term potentiation (LTP) and depression (LTD) of excitatory synapse strength require the Ca(2+)/c

57 long-term potentiation (LTP) and depression (LTD) were significantly reduced in hippocampal slices ta

58 HIPP cells induces long-lasting-depression (LTD) of synaptic transmission but long-term-potentiation

59 on (LTF), and long-term synaptic depression (LTD).

60 lu1/5-induced long-term synaptic depression (LTD).

61 Long-term depression (LTD) (selective weakening of specific sets of synapses)

62 MeA neurons underwent long-term depression (LTD) after theta burst stimulation of the accessory olfa

63 potentiation (LTP) and long-term depression (LTD) and homeostatic scaling.

64 f both corticostriatal long-term depression (LTD) and long-term potentiation (LTP) is proposed to be

65 o determine changes in long-term depression (LTD) and long-term potentiation (LTP) of PFC responses r

66 ired induction of both long-term depression (LTD) and long-term potentiation (LTP).

67 MD selectively induces long-term depression (LTD) and shifts spike timing-dependent plasticity (STDP)

68 rm potentiation (LTP), long-term depression (LTD) and spike-timing dependent plasticity (STDP) are de

69 potentiation (LTP) and long-term depression (LTD) are the two major forms of long-lasting synaptic pl

70 in activity-dependent long-term depression (LTD) at hippocampal Schaffer collateral (SC)-CA1 synapse

71 ial role for ASIC1a in long-term depression (LTD) at mouse insular synapses.

72 In long-term depression (LTD) at synapses in the adult brain, synaptic strength i

73 Long-term depression (LTD) between cortical layer 4 spiny stellate cells and l

74 potentiation (LTP) and long-term depression (LTD) can be induced at the same synaptic activation freq

75 naptic plasticity, the long-term depression (LTD) elicited by activation of type-I metabotropic gluta

76 In contrast, long-term depression (LTD) emerges in the absence of PII activity.

77 potentiation (LTP) and long-term depression (LTD) forms that relay on the activation of NMDA receptor

78 potentiation (LTP) and long-term depression (LTD) in anesthetized mice in vivo.

79 The expression of long-term depression (LTD) in cerebellar Purkinje cells results from the inter

80 (LTP) and facilitated long-term depression (LTD) in PFC pyramidal neurons.

81 potentiation (LTP) and long-term depression (LTD) in principal neurons of the basolateral amygdala (B

82 istribution of Inp54p, long-term depression (LTD) induced by low-frequency stimulation was blocked in

83 on (LTP) is intact but long-term depression (LTD) is impaired in K(b)D(b)(-/-) mice.

84 reased mGluR5-mediated long-term depression (LTD) leading to several clinical trials of mGluR5 inhibi

85 potentiation (LTP) and long-term depression (LTD) mechanisms that rely on the activation of NMDA rece

86 ation of mGlu3 induces long-term depression (LTD) of excitatory transmission in the PFC at inputs fro

87 an inward current and long-term depression (LTD) of glutamate synapses of DRn 5-HT neurons.

88 receptor D4-dependent long-term depression (LTD) of glutamatergic excitatory synapses by increasing

89 ) leads selectively to long-term depression (LTD) of hippocampal-PFC NMDAR-mediated synaptic transmis

90 s) in conjunction with long-term depression (LTD) of synaptic strength.

91 vealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induc

92 internalization during long-term depression (LTD) require clathrin and dynamin, the mechanisms govern

93 potentiation (LTP) and long-term depression (LTD) to assess deficits in bidirectional synaptic plasti

94 vivo circuit-specific long-term depression (LTD) unmasks the therapeutic power of EE to achieve long

95 tentiation (LTP) or of long-term depression (LTD) were assessed using respectively intermittent (iTBS

96 iation (LTP), impaired long-term depression (LTD), and a thinning of the postsynaptic density (PSD) a

97 a critical role in pRh long-term depression (LTD), one of the primary physiological processes thought

98 potentiation (LTP) or long-term depression (LTD), or globally during homeostatic scaling.

99 potentiation (LTP) or long-term depression (LTD), respectively.

100 ptors (mGluRs) induces long-term depression (LTD), which requires new protein synthesis.

101 glutamatergic synaptic long-term depression (LTD), without significant effects on chronic corticoster

102 play impaired cortical long-term depression (LTD).

103 obust activity-induced long-term depression (LTD).

104 potentiation (LTP) and long-term depression (LTD).

105 potentiation (LTP) and long-term depression (LTD).

106 le in the induction of long-term depression (LTD).

107 potentiation (LTP) and long-term depression (LTD).

108 nduced NMDAR-dependent long-term depression (LTD).

109 Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associ

110 pocampal mGluR-induced long-term depression (LTD; or chemically induced mGluR-LTD) in Eif4ebp2(-/-) m

111 d over development to favor LTP and diminish LTD in adults.

112 eals how PTPMEG cooperates with PKC to drive LTD expression by facilitating the effect of PKC on the

113 met during design of ligand-targeted drugs (LTDs) to achieve the required therapeutic potency with m

114 hippocampal synapses by anchored PKA during LTD induction but are then rapidly removed by anchored c

115 for Rab11Fip5, and presumably Rab11, during LTD.

116 iently augment NMDAR Ca(2+) signaling during LTD induction.

117 In contrast, eCB-LTD in PE animals was not rescued by increasing presynap

118 nnabinoid-mediated long-term depression (eCB-LTD) in VTA DA neurons.

119 Together, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primari

120 Mechanistic studies for impaired eCB-LTD revealed that PE downregulated CB1 receptor function

121 stently alters eCB signaling and impairs eCB-LTD at the excitatory synapses, an important synaptic pl

122 educed low-frequency stimulation-induced eCB-LTD.

123 Interestingly, eCB-LTD in PE animals was rescued by metabotropic glutamate

124 potentiation and spine anomalies but not eCB-LTD.

125 ortunities for innovating safe and effective LTDs has never been greater.

126 urin, and T-type Ca(2+) channels will elicit LTD of the activated GABAergic synapses when coupled wit

127 done disrupted mu OP-LTD and endocannabinoid-LTD, but not delta or kappa OP-LTD.

128 ted, differentially occluded endocannabinoid-LTD and inhibited different striatal inputs.

129 t blocked serotonin-induced LTF and enhanced LTD induced by the neuropeptide Phe-Met-Arg-Phe-NH2.

130 to obtain consistent results, especially for LTD in vivo.

131 3-driven gene transcription was required for LTD as inhibition of STAT3-DNA binding, nuclear export,

132 tic, not presynaptic NMDARs are required for LTD induction.

133 for relatively larger calcium transients for LTD than for LTP induction at any given stimulus frequen

134 FC plasticity, characterized by a shift from LTD to LTP without altering the BLA-induced LTP.

135 r synaptic efficacy, which precluded further LTD induction.

136 may result in different consequences (e.g., LTD instead of LTP), according to the initial conditions

137 rained to self-administer cocaine, GABAergic LTD was abolished in D2-, but not in D1-MSN synapses.

138 on at hippocampal CA3-CA1 synapses (O-GlcNAc LTD).

139 ng AMPARs, similar to expression of O-GlcNAc LTD.

140 el form of LTD at CA3-CA1 synapses, O-GlcNAc LTD.

141 It is noteworthy that glutamatergic LTD, which is known to exist on stratum lucidum interneu

142 Rab11Fip5 did, however, abolish hippocampal LTD as measured both in acute slices or using a chemical

143 ry nucleus develop a long-term depression (I-LTD) when challenged by a stimulation paradigm that mimi

144 This I-LTD may be a key element involved in the reshaping of th

145 restingly, VU0453595 fully restored impaired LTD as well as deficits in cognitive function and social

146 The impaired LTD and extinction learning in ASIC1a null mice were res

147 AMPAR GluA1 subunits at sites implicated in LTD.

148 ify a number of candidate miRNAs involved in LTD.

149 ropic versus metabotropic NMDAR signaling in LTD, we examined the effects of varying extracellular Ca

150 ional control, protein synthesis-independent LTD, neocortical hyperexcitability, audiogenic seizures,

151 receptors unmasked 10 Hz stimulation-induced LTD and LTP, respectively.

152 Synaptically induced LTD was deficient in Eif4ebp2(-/-) mice, and this defici

153 abotropic glutamate (mGlu) receptors induces LTD of synaptic transmission at Schaffer collateral-CA1

154 e activation of the M1 mAChR subtype induces LTD in PFC and that this response is completely lost aft

155 restingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative i

156 60, in the absence of APV, no or very little LTD was found in KO that was completely restored by appl

157 LTP, LTD, and homeostatic scaling alter synaptic strength thr

158 lation controls AMPAR trafficking during LTP/LTD.

159 Hence LTP/LTD changes in AD mouse models may reflect defects in me

160 nstrate that the apparent differences in LTP/LTD magnitude seen across ages in AD transgenic mouse mo

161 The initial offset in LTP/LTD threshold in young Tg mice did not accompany changes

162 observed at the soma after induction of LTP/LTD reflects the actual (local) synaptic state.

163 Tg mice did not accompany changes in the LTP/LTD induction mechanisms, but altered AMPA receptor phos

164 To determine this, we examined the LTP/LTD induction threshold in APPswe;PS1DeltaE9 transgenic

165 We found that endocannabinoid/mGlu5-mediated LTD and NMDAR-dependent LTP were lacking in adult n-3-de

166 scovered that endocannabinoid/mGlu5-mediated LTD in the mPFC and accumbens was abolished in adult n-3

167 MDARs and their regulation of mGluR-mediated LTD at different developmental stages using several diff

168 ogy of FXS leading to altered mGluR-mediated LTD.

169 a phenomenon exhibited during mGluR-mediated LTD.

170 , activity-dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSC(NMD

171 dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSC(NMDA)) at the

172 d we observed a profound impairment in mGlu3-LTD following a single, 20-min restraint stress exposure

173 Our data suggest mGlu3-LTD is mediated by postsynaptic AMPAR internalization in

174 mGluR-LTD reduces synaptic strength and is relevant to learnin

175 mGluR-LTD was associated with calpain-1 activation following T

176 ion of GluN2B, but not GluN2A, blocked mGluR-LTD only in WT.

177 Consistent with compromised mGluR-LTD, MK2/3 DKO mice have distinctive deficits in hippoca

178 Consistently, mGluR-LTD was impaired in calpain-1 KO mice, and the impairmen

179 mGluR long-term depression (mGluR-LTD) is a form of synaptic plasticity induced at excitat

180 mGluR-dependent long-term depression (mGluR-LTD), a key biomarker in the disease, at four different

181 eceptor-mediated long-term depression (mGluR-LTD)-whose disruption is postulated to increase vulnerab

182 APC operates in the cytoplasm to drive mGluR-LTD.

183 d late phase of Arc translation during mGluR-LTD, through a mechanism involving mTOR and ribosomal pr

184 t the underlying cause of the enhanced mGluR-LTD in KO (at p30) is caused by dysregulated NMDAR signa

185 cessive protein synthesis, exaggerated mGluR-LTD, and audiogenic seizures.

186 otypical RNA granule substrate and for mGluR-LTD in hippocampal neurons.

187 havioral task that induces hippocampal mGluR-LTD in vivo.

188 he Cdh1 knockout phenotype of impaired mGluR-LTD.

189 complex (Cdh1-APC), profoundly impairs mGluR-LTD in the hippocampus.

190 hat calpain-1 plays a critical role in mGluR-LTD and is involved in many forms of synaptic plasticity

191 merging as important control points in mGluR-LTD, a form of synaptic plasticity that is compromised i

192 , including NMDA receptors (NMDAR), in mGluR-LTD.

193 depression (LTD; or chemically induced mGluR-LTD) in Eif4ebp2(-/-) mice was rescued by mGluR1 or mGlu

194 Interestingly, AKT activity inhibits mGluR-LTD, with overlapping functions for AKT1 and AKT3.

195 activation of Type I mGluRs and, like mGluR-LTD but unlike NMDAR-dependent plasticity, depends cruci

196 ocalization protein STAU2 in mediating mGluR-LTD through the regulation of mRNA translation complexes

197 of LTD that depends on Type I mGluRs (mGluR-LTD), but not NMDARs, has been implicated in learning de

198 Our findings identify a new model of mGluR-LTD, which promises to be of value in the treatment of m

199 ses to be of value in the treatment of mGluR-LTD-linked cognitive disorders.

200 pe-I metabotropic glutamate receptors (mGluR-LTD).

201 rome, but the mechanisms that regulate mGluR-LTD remain incompletely understood.

202 uitin signaling pathway that regulates mGluR-LTD in the brain.

203 n the KO where blocking GluN2B rescued mGluR-LTD, suggesting GluN2B-containing NMDARs in the KO are h

204 At all other age groups tested, mGluR-LTD was almost identical between KO and WT.

205 ected, in the presence of APV, we found more LTD in the mouse KO than in WT.

206 Because most LTDs are composed of a targeting ligand (e.g., organic m

207 Consistent with altered NAc LTD, TLR4.KO animals exhibit an attenuation in drug rewa

208 this association because pHFD abolishes NMDA-LTD, a function that is restored by RELN overexpression.

209 partate-dependent long-term depression (NMDA-LTD) at prefrontal excitatory synapses as a synaptic sig

210 ceptor-dependent long-term depression (NMDAR-LTD), a prototypic form of synaptic plasticity, is accom

211 ying long-lasting spine remodelling in NMDAR-LTD, however, are largely unclear.

212 at antagonism of mGlu5 inhibits LTP, but not LTD at MF synapses of freely behaving adult rats.

213 ns of Delta(9)-tetrahydrocannabinol occluded LTD compared with vehicle injections; however, a single

214 f a protein synthesis-dependent component of LTD, normalization by mGluR1 antagonists requires the ac

215 Subsequent optogenetic delivery of LTD conditioning to the auditory input inactivates memor

216 (1 month), LTP is enhanced at the expense of LTD, but in adults (6 months), the phenotype is reversed

217 ion, long-term potentiation or expression of LTD.

218 pruning in the context of recent findings of LTD dysregulation in several mouse models of autism spec

219 sing O-GlcNAcylation induces a novel form of LTD at CA3-CA1 synapses, O-GlcNAc LTD.

220 However, only the mGluR-dependent form of LTD has been characterized.

221 In young rodents, this form of LTD has been repeatedly reported to require presynaptic

222 Indeed, dysfunction of a form of LTD that depends on Type I mGluRs (mGluR-LTD), but not N

223 Several forms of LTD involving activation of different presynaptic Gi/o-G

224 ragment can be explained by an impairment of LTD and LTP at the parallel fiber-to-PC synapse and alte

225 and STAT3 accompanied chemical induction of LTD and AMPA receptor internalization.

226 selective potentiation of M1 on induction of LTD and behavioral deficits in PCP-treated mice.

227 , our results indicate that the induction of LTD in the hippocampal CA1 region is dependent on ionotr

228 PIP2 is critically required for induction of LTD whereas translocation of Inp54p to plasma membranes

229 ASIC1a reduced the induction probability of LTD without affecting that of long-term potentiation in

230 f specific sets of synapses) and reversal of LTD were present, although impaired, in adolescence and

231 olitis) were associated with a lower risk of LTD (unadjusted hazard ratio [HR], 0.62; P < .001 and HR

232 sex was also associated with a lower risk of LTD or malignancy (HR, 0.88; P = .002 and HR, 0.68; P <

233 duct PSC was associated with a lower risk of LTD or malignancy compared with classic PSC (HR, 0.30 an

234 Studies of LTD mechanisms have focused mainly on postsynaptic AMPA-

235 king NMDAR channel ion fluxes with MK-801 on LTD and NMDAR signaling in the mouse hippocampal CA1 reg

236 Mu and delta OP-LTD, although both being presynaptically expressed, were

237 Kappa OP-LTD showed a unique subregional expression in striatum.

238 docannabinoid-LTD, but not delta or kappa OP-LTD.

239 e opioid analgesic oxycodone disrupted mu OP-LTD and endocannabinoid-LTD, but not delta or kappa OP-L

240 However, optogenetic LTD applied to this projection in vivo transiently re-si

241 Instructive signals determine whether LTP or LTD is induced, by modulating local calcium transients.

242 vanished >50 Hz or <1 Hz (where only LTP or LTD occurred).

243 vidual synapses expressed significant LTP or LTD, but the average over all synapses did not change.

244 ke cortical plasticity forming a paradoxical LTD in comparison to HS.

245 ur model advances the understanding of PF-PC LTD regulation and induction, and provides a validated e

246 somatodendritic profiles throughout the PPT/LTD complex.

247 export, and gene transcription all prevented LTD induction.

248 Conversely, mGlu5 antagonism prevents LTD but not LTP at AC-CA3 synapses.

249 both frequencies, buffering calcium prevents LTD induction and LTP results instead, identifying the e

250 ynaptic, but not presynaptic NMDARs prevents LTD induction.

251 ion of GluN2B receptors would compromise pRh LTD, leading to loss of NOR memory.

252 ation resulted in an inability to induce pRh LTD following 1 Hz stimulation, an effect that was rever

253 Ro 25-6981 prevented DCS restoration of pRh LTD in meth subjects.

254 Thus, targeting pRh LTD may be a promising strategy to treat meth-induced co

255 onths), the phenotype is reversed to promote LTD and reduce LTP, compared to age-matched wild-type (W

256 her enhances calcium transients and promotes LTD.

257 CA1 region of the hippocampus, GRF1 promotes LTD, whereas GRF2 promotes theta-burst stimulation-induc

258 scribed AKAP79/150 trafficking in regulating LTD-induced spine shrinkage.

259 MPA receptors Ca(2+) impermeable and rescues LTD.

260 Optogenetic stimulation designed to saturate LTD produced the same impairment in WT as observed in DK

261 Both st-LTP and st-LTD required NMDA receptors, but st-LTP also required re

262 Importantly, st-LTP and st-LTD were significantly larger than LTP and LTD obtained

263 m potentiation and depression (st-LTP and st-LTD) were confined to a +/-25 ms time-window.

264 led APs in st-LTP while APs led EPSPs in st-LTD, STDP was Hebbian in nature.

265 ession results in impaired mGluR5-stimulated LTD.

266 Notably, such LTD-induced depalmitoylation was also blocked by CaMKII

267 ulopontine (PPT) and laterodorsal tegmental (LTD) nuclei of the mesopontine tegmentum (MPT).

268 Here we demonstrate that LTD at adult TA-CA1 synapses involves JAK-STAT signaling

269 ntive and discriminative roles, we find that LTD at the dorsal ITC is impaired in mice exhibiting PTS

270 In further support of the idea that LTD has preventive and discriminative roles, we find tha

271 Model simulations show that LTD expression is increased by serine/threonine phosphat

272 Here we review evidence suggesting that LTD and synaptic pruning share components of their under

273 The LTD by single pyramidal cell 40 Hz spike bursts is speci

274 The LTD of VLE connections alters suprathreshold activation

275 The LTP-like effects of PAS25 and the LTD-like effect of PAS10 were both significantly enhance

276 ether LTD or LTP is evoked but, instead, the LTD threshold slides, thus preserving the requirement fo

277 of these mRNAs, oligophrenin-1, mediates the LTD induced by eIF2alpha phosphorylation.

278 receptors was responsible for occluding the LTD.

279 te significantly to the decisive role of the LTD and PPT in sleep-wakefulness.

280 h priming and following cTBS150 reversed the LTD-like effect produced by PAS10 with little change in

281 Disruption of this LTD could contribute to the rigid emotional and motivati

282 centered on the dorsal ITC reveal that this LTD limits less salient experiences from forming persist

283 Thus, LTD in HIPPs may assist flow of spatial information from

284 Here, we show that, in contrast to LTD, constitutive AMPAR internalization and homeostatic

285 ir subunit composition and susceptibility to LTD.

286 ke timing-dependent plasticity (STDP) toward LTD at GABAergic synapses onto VTA DA neurons through ep

287 er-Purkinje cell synapses, which can undergo LTD or LTP in response to 1-Hz and 100-Hz stimulation.

288 , while MF glutamatergic responses underwent LTD, the simultaneous MF GABAergic responses of stratum

289 ctivation and reactivation of a memory using LTD and LTP, supporting a causal link between these syna

290 inhibitory GABAergic synapses and an in vivo LTD of excitatory glutamatergic synapses.

291 at favors phosphorylation by prolonged, weak LTD stimuli versus brief, strong LTP stimuli.

292 h actually led to LTP in PE animals, whereas LTD was still observed in controls.

293 ith high intracellular cAMP and LFS, whereas LTD required low intracellular cAMP and high-frequency s

294 augmented by twofold in R192Q mice, whereas LTD was unchanged compared with wild-type mice.

295 eferentially induced at MF synapses, whereas LTD is favored at AC synapses.

296 te calcium amplitudes that determine whether LTD or LTP is evoked but, instead, the LTD threshold sli

297 spectrum disorder (ASD) and discuss whether LTD deficits can indicate impaired pruning processes tha

298 hysiologically plausible explanation for why LTD induction is experimentally difficult to obtain.

299 ere that the spine shrinkage associated with LTD indeed requires synaptic AKAP79/150 removal, which i

300 itment, removal, or activity interferes with LTD.